• Biomolecules & Therapeutics
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• v.13 no.3
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• pp.133-137
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• 2005

Wogonin(5,7-dihydroxy-8-methoxyflavone), an anti-inflammatory plant flavonoid, was previously demonstrated to modulate the several parameters of animal skin inflammation. This compound inhibited edematic response as well as proinflammatory gene expression. In this investigation, the histopathological changes of the lesions from different types of experimental skin inflammation were compared and the potential therapeutic effect of topically applied wogonin was evaluated. From the results, it was found that multiple TPA treatment drastically increased ear edema accompanied with epidermal hyperplasia and inflammatory cell infiltration, while phenol treatment provoked only edematic response in the dermal area. Wogonin somewhat differently inhibited these animal models of skin inflammation.

• Korean Journal of Clinical Pharmacy
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• v.14 no.2
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• pp.71-77
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• 2004

The author has tested the clinical efficacy and safety of an anti-inflammatory drug in patients with inflammation of the otnrhinolaryngology. Deoxyribonuclease prepared from bovine pancreas destroyed fibers and reduced the viscosity of the exudates. Bromelain is a group of proteolytic enzymes which are known to have an effect on inflammation, swelling, and pain in inflammatory disorders. The mucolytic and anti-inflammatory properties of deoxyribonuclease associated with bromelain in inflammation of otorhinolaryngology were assessed in 67 patients. A standard dose of 3 tablets of deoxyribonuclease bromelain tablet was given for not less than 7 days. In all tile groups of patients considered, the drug showed a considerable therapeutic effectiveness. At the end of 7-28 days treatment, more than $89.6\%$ of treatment was improved. These findings suggest that it could be permitted to use deoxyribonuclease-bromelain tablet in patients with inflammation of the otorhinolaryngology.

• Journal of Veterinary Clinics
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• v.5 no.2
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• pp.83-86
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• 1988

Morphometric observation on the ovarian follicles of ICR strain-female mice has been conducted to investigate the effect of induced inflammation on the follicular populations. Inflammation was induced by administering 25${\mu}\ell$ of turpentine oil intraperitoneally 2 times at the interval of 3 days. Mice showing 5-day estrous cycle about 20 days after induction of inflammation are placed in experimental group. Normal follicles of 100～399$\mu\textrm{m}$ in diameter increased at estrus but those of over 400$\mu\textrm{m}$ decreased. super-ovulation increased the number of normal follicles of over 400$\mu\textrm{m}$. The number of normal follicles of over 400$\mu\textrm{m}$ 48 hours after superovulation was not significantly different between experimental and control groups. Present results indicated that the number of preovulatory follicles 48 hours after PMSG injection did not decrease in the mice which showed regular estrous cycle even after the induction of inflammation.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.15 no.1
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• pp.50-62
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• 2002

In the age of puberty or 20-30th young people who are sensitive to outward appearance, acne is serious problem at beauty and has social and psychological influence on that people. So this experiment is carried out for test whether the addition temperament drugs of Yungyopaedock-san(YP) have an anti-inflammatory effect and have suppression effect on immunocyte in the state of inflammation which induced by acne. The results was as follows. 1. YP has suppress inflammatory reaction induced by carageenan. 2. YP has suppress increasing activation of abdominal cavity macrophage in the carageen and zymosan induced inflammation. 3. YP has suppress increasing activation of spleen cell in the carageenan and zymosan induced inflammation. Based on the above result, YP was improved its suppression effect to the inflammatory reaction through the suppression of spleen cell and macrophage activation. So we concluded that YP is prospected as a anti-inflammatory agent to cure inflammation induced by ance.

• Tuberculosis and Respiratory Diseases
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• v.80 no.4
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• pp.325-335
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• 2017

Chronic obstructive pulmonary disease (COPD) is associated with abnormal inflammatory response and airflow limitation. Acute exacerbation involves increased inflammatory burden leading to worsening respiratory symptoms, including dyspnea and sputum production. Some COPD patients have frequent exacerbations (two or more exacerbations per year). A substantial proportion of COPD patients may remain stable without exacerbation. Bacterial and viral infections are the most common causative factors that breach airway stability and lead to exacerbation. The increasing prevalence of exacerbation is associated with deteriorating lung function, hospitalization, and risk of death. In this review, we summarize the mechanisms of airway inflammation in COPD and discuss how bacterial or viral infection, temperature, air pollution, eosinophilic inflammation, and concomitant chronic diseases increase airway inflammation and the risk of exacerbation.

• Journal of Ginseng Research
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• v.43 no.3
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• pp.335-341
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• 2019

Background: Inflammation is a host-defensive innate immune response to protect the body from pathogenic agents and danger signals induced by cellular changes. Although inflammation is a host-defense mechanism, chronic inflammation is considered a major risk factor for the development of a variety of inflammatory autoimmune diseases, such as rheumatic diseases. Rheumatic diseases are systemic inflammatory and degenerative diseases that primarily affect connective tissues and are characterized by severe chronic inflammation and degeneration of connective tissues. Ginseng and its bioactive ingredients, genocides, have been demonstrated to have antiinflammatory activity and pharmacological effects on various rheumatic diseases by inhibiting the expression and production of inflammatory mediators. Methods: Literature in this review was searched in a PubMed site of National Center for Biotechnology Information. Results: The studies reporting the preventive and therapeutic effects of ginseng and ginsenosides on the pathogenesis of rheumatic diseases were discussed and summarized. Conclusion: Ginseng and ginsenosides play an ameliorative role on rheumatic diseases, and this review provides new insights into ginseng and ginsenosides as promising agents to prevent and treat rheumatic diseases.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.155.3-156
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• 2003

Flavonoids from plant origin show anti-inflammatory activity in vitro and in vivo. In addition to inhibition of inflammation-associated enzymes such as cyclooxygenases and lipoxygenases, they have been found to regulate the expression of inflammation-associated proteins from in vitro experiments. In order to prove in vivo behavior and the potential for beneficial use against inflammatory skin disorders, the effect of wogonin (5,7-dihydroxy-8-methoxyflavone) on in vivo expression of several inflammation-associated genes was examined in the intact as well as in the inflamed mouse skin by reverse transcriptase-polymerase chain reaction analysis. (omitted)

• IMMUNE NETWORK
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• v.22 no.1
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• pp.13.1-13.14
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• 2022

Chronic inflammation plays a critical role in the development of obesity-associated metabolic disorders such as insulin resistance. Obesity alters the microenvironment of adipose tissue and the intestines from anti-inflammatory to pro-inflammatory, which promotes low grade systemic inflammation and insulin resistance in obese mice. Various T cell subsets either help maintain metabolic homeostasis in healthy states or contribute to obesity-associated metabolic syndromes. In this review, we will discuss the T cell subsets that reside in adipose tissue and intestines and their role in the development of obesity-induced systemic inflammation.

• Journal of Korean Society for Atmospheric Environment
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• v.18 no.E2
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• pp.121-128
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• 2002

This study was carried out to investigate if nitric oxide synthase (NOS) inhibitors modulate airway inflammation induced by diesel exhaust particles (DEP). N$\^$G/-nitro-L-arginine methyl ester (L-NAME), a potent constitutive NOS (cNOS) inhibitor, and aminoguanidine (AG), a selective inducible NOS (iNOS) inhibitor, were administered to mice in their drinking water for 7 weeks. Airway inflammation was elicited by the repeated intratracheal administration of DEP. The results showed that macrophages, inflammatory eosinophils and neutrophils in bronchoalveolar lavage (BAL) fluids by intratracheal DEP instillation were significantly suppressed in the mice treated with two NOS inhibitors toghther with DEP. The suppression of these cells was more effective in AG treated groups than in L -NAME treated groups. NOS inhibitor treatment also reduced interleukin -5 (IL-5 in the BAL fluids and lung homogenates. Additionally, it was found that eosinophil peroxidase (EPO) activity in the BAL fluids was also decreased by NOS inhibitor treatment. These results suggest that nitric oxide (NO) is produced in airway inflammation by repeated DEP instillation, and that iNOS inhibition as well as cNOS inhibition can play a modulating role in this airway inflammation by DEP.

• IMMUNE NETWORK
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• v.12 no.5
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• pp.176-180
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• 2012

Although the majority of research on CD137 has been directed to T cells, it is becoming clear that this molecule has distinct functions in other lineages of cells, including non-hematopoietic cells. In particular, emerging evidence suggests that the CD137-its ligand (CD137L) network involving immune cells and non-immune cells, directly or indirectly regulates inflammation in both positive and negative manners. Bidirectional signaling through both CD137 and CD137L is critical in the evolution of inflammation: 1) CD137L signaling plays an indispensible role in the activation and recruitment of neutrophils by inducing the production of proinflammatory cytokines and chemokines in hematopoietic and non-hematopoietic cells such as macrophages, endothelial cells and epithelial cells; 2) CD137 signaling in NK cells and T cells is required for their activation and can influence other cells participating in inflammation via either their production of proinflammatory cytokines or engagement of CD137L by their cell surface CD137: 3) CD137 signaling can suppress inflammation by controlling regulatory activities of dendritic cells and regulatory T cells. As recognition grows of the role of dysregulated CD137 or CD137L stimulation in inflammatory diseases, significant efforts will be needed to develop antagonists to CD137 or CD137L.